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Breast Surgery - Science topic

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More women in the U.S. are choosing to have their breasts removed for early cancers instead of breast-conserving procedures that deliver equal results, according to a new study.
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I am working on my MSc dissertation, investigating breast protection bras for female boxers. I am looking at their protection but also the fit and shaping of them and how this relates to their comfort during wear. Is there any sort of classification of the shape of women's breasts? How would I describe the natural breast shape?
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Thank you
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What's the verdict on regional analgesia in breast surgery?
Is there any need to use it at all?
The 2018 Cochrane review concluded that synthesis of 18 RCTs favoured regional anaesthesia for the prevention of persistent pain three to 12 months after breast cancer surgery with an OR of 0.43 (95% CI 0.28 to 0.68, 1297 participants, low‐quality evidence).
However, the recent 11-year RCT published in the Lancet 2019 with 2132 patients across 13 hospitals internationally showed there was no difference in incisional pain:
Incisional pain was reported by 442 (52%) of 856 patients assigned to regional anaesthesia-analgesia and 456 (52%) of 872 patients allocated to general anaesthesia at 6 months, and by 239 (28%) of 854 patients and 232 (27%) of 852 patients, respectively, at 12 months (overall interim-adjusted odds ratio 1·00, 95% CI 0·85-1·17; p=0·99). Neuropathic breast pain did not differ by anaesthetic technique and was reported by 87 (10%) of 859 patients assigned to regional anaesthesia-analgesia and 89 (10%) of 870 patients allocated to general anaesthesia at 6 months, and by 57 (7%) of 857 patients and 57 (7%) of 854 patients, respectively, at 12 months.
If it doesn't reduce chronic post surgical pain, is there any point in using it?
(Note: these studies involved paravertebral regional analgesia)
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In high risk patients para vertebral block in T2 and T4 level with or without serratus anterior plane block MRM can be done.. should be done under light sedation...
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Hi all,
I need to know if there is any ongoing research on avoiding surgery after neoadjuvance (qt+rt) for breast cancer.
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The study of reliability of Biopsy post NACT is out. Clinical Complete resposnse include radiologically no evidence of tumour. These patients were biopsied in tumour bed, guided by tumour marker placed when tumour was palpable!
It turn out that such biopsies are unreliable to detect possible viable tumour!
So for Now, one cannot avoid surgery post NACT, even if there is clinical complete response! Surgery remains most important tool for cure of breast cancer.
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Plastic surgery,  Breast surgery, Breast implants 
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Do you mean temporising saline implants?
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So it is somewhat understood that a sentinel node biopsy after lumpectomy or a previous sentinel is contraindicated considering that the lymphatic supply is compromised already and it can lead to false negative results.  A myth or not?
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I agree, it may difficult its localization but It does not contraindicate it
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I have 38 old fm patient. Family history (+). 3 years ago we perfomed bilateral risk reduction mastectomy after a diagnosis of LCIS. Mastectomy was done with nipple sparing technique and retromuscular Becker prothesis. the follw up was uneventful until 1 month ago. Patient had a skin rash at his left breast inner quadrant. The biopsy of this area confirmed a invasive ductal tumor. The area contains 1/3 of his breast and have extension to the other breast .
do you prefer Surgery or a neoadjuvant chemo ?
should we the prothesis take don
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Last weeks we have began a chemo to the patient. I'll give information about the progress after chemo treatment.
Thanks to colleges that share knowledge with me
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Does any one knows any actual randomised trial to check on breast cancer recurrence after pectoralis fascia preservation?
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There is no evidence to support routine excision of either skin overlying the tumor or fascia underneath the tumor when margins are otherwise adequate.
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A 41 yrs old woman with a 2*2 cm in UOQ left breast cancer and reactive node in axial at USO. Her mother  had breast cancer at 50 yrs and BRCA mutation.Mamography  showed only mass.What is your plan Mastectomy or BCT?
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NCCN Guidelines Version 1.2016 Invasive Breast Cancer
SPECIAL CONSIDERATIONS TO BREAST-CONSERVING THERAPY REQUIRING RADIATION THERAPY Contraindications for breast-conserving therapy requiring radiation therapy include:
Absolute:
• Radiation therapy during pregnancy
• Diffuse suspicious or malignant-appearing microcalci cations
• Widespread disease that cannot be incorporated by local excision through a single incision that achieves negative margins with a
satisfactory cosmetic result 1 • Diffusely positive pathologic margins
Relative:
• Prior radiation therapy to the chest wall or breast; knowledge of doses and volumes prescribed is essential. • Active connective tissue disease involving the skin (especially scleroderma and lupus)
• Tumors >5 cm (category 2B)
• Positive pathologic margin1
Women with a known or suspected genetic predisposition to breast cancer:
May have an increased risk of ipsilateral breast recurrence or contralateral breast cancer with breast-conserving therapy Prophylactic bilateral mastectomy for risk reduction may be considered.
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Serratus block is effective for mastectomy and also for axillary dissection? And I don't understand clearly the difference between Serratus and PEC's 2 (the injection of anesthetic is upper or underneath of serratus muscle?).
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Serratus block is effective
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There are some patients with bulky and multifocal or multicentric breast cancer that with oncoplastia techniques could benefit of conservative surgery, I would like to know about this topic experiences.
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Quadrantectomy as a form of conservative breast surgery is acceptable in cases of MF tumors, because all tumor foci can be removed specially if breast volume is good in comparison to tumor volume. We suggest NSM with SLNB in all cases of suspected MC tumors . Lobular histology most commonly associated with multicentric breast cancer.
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I am interested to learn more regarding Kinesio taping efficacy on lymphoedma especially in cancer patients.
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Thank you Mr.Tamer
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Plastic surgery, Plastic and Reconstructive Surgery,  Breast surgery 
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Capsule formation Baker III and IV has nothing to do with the surface of the implants- it is merely due to slow infection with Biofilm producing bacteria, mostly St. epidermidis of the patient ! Read the recent literature on Breast Implants and  Biofilm (abstracts at www.pubmed.gov)  and use the more natural feeling of silicone gel filled implants with natural feeling - and a vial of antibiotics (any cephalotin) into the implant pocket at the end of the operation . 
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A patient underwent Hadfield procedure and was found to have high grade DCIS with several tiny foci of invasive ductal carcinoma. Now i need to do sentinel lymph node biopsy. Normally i do peri-aerolar injection of the dye. However, it is not possible in this case. Where should the dye be injected?
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Dear Dr Ramawad
we had similar patients and we inject TC radio tracer  and blue dye (isosulfan blue) subdermaly at the ends of scar .
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I mean: in order to have clear margins at extemporaneous pathological examination. You stick to preoperative design of removal? Use intra-operative ultrasound? Aim larger margins?...
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The best recipe to have negative margins when removing a breast lesion of uncertain nature  is the incision  1 cm 
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I'm interested in nonrandomized, controlled trials, if any are available. I've been searching for such a study(ies) and have had no luck. I found anecdotal evidence and several nursing articles explaining post-op protocols (with no sources to back the protocols up). 
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I think there are less evidence about that. I´ve found this interesting article for my students. I hope helps you a little.
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Lipofilling or lipotransfer is a relatively new method to do secondary correction of smaller partial mastectomy defects after breast-conserving therapy of breast cancer. Do patients have an increased risk for local recurrences after lipofilling or is it a safe procedure in breast cancer patients ?
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We don´t know yet. We know that lipofilling and the herein contained preadipocytes (MST) in vitro can promote tumor growth.
Therefor, in a lot of countries (like France and Germany) Lipofilling after breast conserving therapy, which in itself implies that there may be tumorous tissue left behind, lipofilling, for now, should not be performed.
future will tell.
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For the post masterctomy/lumpectomy radiation therapy, can someone enlighten me with the step-by-step procedure for reconstruction/radiation? I am not sure I fully understand the concept of "immediate reconstruction" - dose this mean implant without radiation? In addition, what dose "implant only" mean in this type of procedure? The radiation comes first, or the reconstruction comes first and then radiation?
Many thanks.
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One-stage immediate breast reconstruction may be done at the same time as mastectomy. After the general surgeon removes the breast tissue, a plastic surgeon places a breast implant.
Two-stage reconstruction or two-stage delayed reconstruction is the type most often done if implants are used.An implanted tissue expander, which is like a balloon, is put under the skin and chest muscle. Through a tiny valve under the skin, the surgeon injects a salt-water solution at regular intervals to fill the expander over a period of about 4 to 6 months. After the skin over the breast area has stretched enough, a second surgery will remove the expander and put in the permanent implant.
The two-stage reconstruction is sometimes called delayed-immediate reconstruction because it allows time for other treatment options. If the surgical biopsies show that radiation is needed, the next steps may be delayed until after radiation treatment is complete. If radiation is not needed, the surgeon can start right away with the tissue expander and second surgery.
if you  plan  RT for your patient  you have two chance
1- tissue expander ---RT--- breast implant 
2- flap procedures; A pedicle flap or a free flap ( TRAM,LD )
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I had a mastectomy for a 4 cm invasive Ductal CA on a 40 years old lady with sentinel node biopsy.Unfortunately frozen section instrument got a problem and we closed the wound without formal axillary dissection.Now I knew that 3 of 4 sentinel node was positive.Is it essential to do a formal axillary dissection in this patient?
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Dear Bijan,
certainly there is an indication for complete axillary dissection, since 4 and more nodes involved would implicate dose-dense chemotherapy. Thus, it has clearly therapeutic relevance to know the exact extent of axillary node involvement.
All the Best
Rainer
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presently skin excision is the answer for simon 's grade 3 gynecomastia for good cosmetic results 
can anyone suggest if any other treatment guidelines available
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When skin excision is necessary I usually prefer to do inferior pedicle. As a result the final scar is located in the IMF and there is no horizontal scar on the left and right of the areola.
The technique is well described in a plastic surgery book by Peter Neligan.
However, especially in young patients two stages should be considered. After liposuction many patients are happy with the result and they don’t want to proceed to further operation.
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As compared with autologous fat transfer breast auto-augmentation. Could these two techniques be combined ?
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To answer your question,it must be simplified at first:a-how much is the breast volume of the patient? b-the degree of mastoptosisi(if  it is present)
Benelli mastopexy is a gold standart in ptotic breasts,especially there was no volume problem..If there is hypoplasia, one of the following methods may be selected: 1-implant,2-adipofacial flap transfer 3-Free Dermal fat transfer 4-Autologous Fat transfer(injection) with or withouth BRAVA vacum aplicator ..To my opinion,selection should be made by individual characteristics of each patient.
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Measuring 'quality' in surgery has become important, as its only with measuring 'quality' that we can begin to make improvements in care.   Various measures have been suggested, such as 
Mortality
Length of stay
Reoperation rate
Readmission rate
Intra-operative injury rate (for example CBD injury / ureteric injury)
Rate of laparoscopic surgery
Rates of conversion to open surgery
to be measured to compare quality in surgery specifically.
Lots of these factors can vary naturally, with a hospitals patient population (rich, poor, age group, comorbidities, hospital size, urban, rural, delays in presentation, access to healthcare etc) and other factors such as surgeon training / experience etc and many other reasons.    So variability in these factors is to be expected.
What makes a good 'quality marker' in surgery?
Your thoughts would be appreciated. 
All the best
Ewen
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Very very excellent question! The same as what I want to ask.
It's true as indicated by above answers that in a broad sense, surgical quality could be evaluated by numerous layers of parameters: blood loss, postoperative recovery, pain, patient experience, you name it. I can assure you, viewing in this bird-view angle, it is impossible to evaluate surgical quality or the quality of a surgeon.
Answer my question first: what is a SURGEON? What makes you different from other physicians? What makes you proud of what you are doing?--- Yes! SURGERY! YOU ARE "FIXING" A LIVING PERSON AND SAVING LIFE WITH YOUR KNIFE AND NEEDLES!!!
A long time ago, it was said that a surgeon should have "eagle's eyes, a lion's heart, and women's hands". I was inspired by these words and struggled out of my country to come here to join the team of the best. I don't know how many of you guys still remember this verse, but I'm sure no one is paying any attention to it. However, from my "stupid" point of view, this is EXACTLY the parameters you MUST look for to qualify a surgery and a surgeon--- A profound vision into surgical science, a superior knowledge-based decision maker, and the finest skillful craftsman with prudent responsibility. This is the core parameter that decides the outcome of a surgery. This decides all other above mentioned measures. Yet you are asking: how to measure these?!
I tell you, it's very simple, but I'll ask: do you DARE and do you really CARE? All these properties boils down to only one element: "Surgical skill". If a surgeon, who loves surgery, looks at his operation from the point of view of a craftsman, he would die to make his surgery flawless. And a flawless operation will beat all the indirect measurements like hospital stay, patient feeling, what-so-ever! In such an advanced world, this is very easy to achieve: every surgery should be recorded with video and sound, then reviewed anonymously by a board of superior surgeons. Scores placed on intraoperative bleeding, intraoperative decision making, collateral damage level, surgical cleanliness, intraoperative patient status, suturing skill, tying skill, incision skill, fine movement of instruments, etc. I'll assure you, if you really do so, you will see a tremendous difference between our current attendings. You will be shocked to see why some guy is still working here! How he was selected to be a surgeon!? So answer my question: do you dare to?
Quality control by this means would be most efficient and cost-effective, because this catches problems in ahead, instead of wasting resources to "manage" them after they do occur, which though is the requirement of "evidence-based-medicine", correct? :) LOL
Unfortunately, the quality of surgeons is drifting downwards these years globally. We have a saying: " to attend to the superficials and neglect the essentials". Way too much emphasis placed on candidates' communication skills and their ability to handle textbook knowledge or even their research experiences, but ignoring the most important part of a surgeon: his potential on mastering surgical skills. We are producing more speakers instead of doers. I was told that surgical skill is not viewed as an essential part of surgery......
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Any RCTs? In assessing the success of per-cutaneous needle aspiration for breast abscesses, part of exclusion criteria has been size (larger than 3cm or 5cm diameter according to different authors). Is there anyone with information about which of the two is a superior predictor of failed needle aspiration?
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'Size or locularity'  as  you  asked  above  appears  to  be  a  researcher  bias  to  me.
The  researcher  should  set  out  to find  out  what  factors (not  size  or  locularity) contribute  to  failed  per-cutaneous  drainage  of  breast  abscesses.
You  might  be  surprised  to  discover  a  factor  such  as  poor  technique.
In  my  opinion,   even  if  you  find  out  the  factor  that  has  a  higher   rate it  cannot  be  extrapolated  for  every  centre  or  environment  until  you  have  properly  tackled  the  issue  of   technique  which  might  crop  in  as  a  confounding  variable.
Thank  you.
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Correction of gynecomastia.
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Sharpe [1] and colleagues used the National Cancer Data Base to study the effect of bilateral mastectomy for early-stage breast cancer on length of hospital stay, readmission rate, 30-day mortality, and time to adjuvant therapy.
The authors begin by acknowledging the recent increase in bilateral mastectomies for patients diagnosed with early-stage breast cancer, a trend that is entirely driven by patients rather than experts. They also point out that surgeons typically address reasons for and possible benefits of different procedures and often leave out the possible (unintended) harm caused by such procedures or options. In this case, it is important for clinicians to figure out whether a delay in the initiation of chemotherapy could result in harm.
Longer wait times may be related to the practice of obtaining additional preoperative imaging with MRI, or consultations with plastic surgery or genetic specialists for second opinions. National guidelines from the National Comprehensive Cancer Network and the National Quality Forum recommend adjuvant chemotherapy to be administered within 120 days of diagnosis of breast cancer.
What is your opinion?
 
Reference: 
1. Sharpe SM et al. Impact of Bilateral Versus Unilateral Mastectomy on Short Term Outcomes and Adjuvant Therapy, 2003-2010: A Report from the National Cancer Data Base. Ann Surg Oncol. 2014 Apr 12. 
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There should be a great deal of emphasis on high quality pre-operative consultation for these patients and highly integrated services between breast surgeons, reconstructive plastic surgeons (like me) and oncologists.  Many patients I see, once they have all the relevant information, decided against contralateral prophylactic mastectomy, but the timliness and quality of consultation is vital.  In those patients who do benefit from bilateral mastectomy and reconstruction, as long as the services are well integrated the procedure should be able to be performed without any delay to adjuvent therapy.  Saying this, it is my preference to save immediate reconstruction for those who have DCIS only or have no disease but a high genetic risk. 
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I am working in breast cancer research, comparing Luminal A, Luminal B to TNBC cell lines. I see that some of the Luminals share characteristics of TNBC. I wonder if we should compare all Luminals to TNBC or should we stratify luminals?
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Hamed:
TALE OF TWO GENERATIONS OF MOLECULAR CLASSIFICATION OF BREAST CANCER
The facts are considerably more complicated than so far suggested, although the contributions above are a good start for what is now, in hindsight, seen as the first generation of molecular classification, that is, molecular "taxonomy" of breast cancer into distinct subclasses, pioneered by the Charles Perou and Therese Sørlie team at Stanford University almost a decade and a half ago. But we are already almost five years into the second generation of what I call breast cancer MOLECULAR ARCHITECTURE, the era of breast cancer SUBTYPING (as opposed to first generation SUBCLASSING or subgrouping) developed by Brain Lehmann and his team at the Vanderbilt-Ingram Cancer Center of Vanderbilt University in late 2010, and first published in 2011. This leads to the era of TNBC SUBTYPING for triple negative breast cancer, now well-validated through gene expression profiling, and with, as I will show, validated clinical relevance to the treatment of TNBC disease.
So being a specialist in triple negative breast cancer, I will here try to provide a more complete and up-to-date account of the architecture of TNBC. The first thing to recognize is that although the Perou/Sørlie team in its original seminal classification of breast cancer molecular subtypes [1] did not identify other than an luminal A and luminal B subgroups of the luminal class/subtype, they later [2] suggested a third luminal subgroup, the luminal C tumors. However a subsequent and more definitive analysis [3] of the expanded dataset by the same team wholly failed to support the existence of this third subgroup (luminal C), and without any confirming data to date, the classification of the luminal C subgroup must be considered abandoned as it has been by the authors themselves, as witness in their recent work [4] which now only identifies these breast cancer intrinsic subclasses (and as this paper [4] supersedes - and even contradicts - their previous papers, I would advise using only it, and their later papers (2011 and on) and not the earlier articles):
(1) LUMINAL A (ER+/PR+/HER2-),
(2) LUMINAL B (triple-positive: ER+/PR+/HER2+),
(3) HER2 (ER-/PR-/HER2+),
(4) BASAL (proximately mapped to triple negative: ER-/PR-/HER2- but with defining EGFR+, CK 5/6, and high Ki-67),
(5) CLAUDIN-LOW (triple negativity but with defining E-cadherin, claudin-3, claudinin-4 and claudinin-7 low, and low Ki-67), and I note that this claudin-low subtype has the genomic characteristics of a cancer stem cell-like (CSC) phenotype [5].
(a classification that has been further refined by other investigators).
But the second issue is to note a mistranslation here: preclinical in vitro/in vivo research has typically failed to distinguish between basal tumors, which are proximately mapped to triple negative: ER-/PR-/HER2-, on the one hand, and claudin-low tumors on the other, yet these behave differentially clinically and perhaps also prognostically. Thus, compared to basal-like tumors, claudin-low tumors appear to have lower rates of pCR [6], and so cannot be casually, and carelessly, lumped into "TNBC" cell lines like MB-MDA-231 and others.
THE PROBLEMS OF PRECLINICAL RESEARCH VERSUS MOLECULAR SUBCLASSES
One final example will serve to suggest the vast scope and potential of mistranslations: Many studies on potentially active agents for triple negative breast cancer disease have been conducted using, indifferently, either MDA-MB-231 or MD-MD-468 cells. However MDA-MB-468 cells most closely map basal tumors (EGFR-positivity and cytokeratins 5/6) while MDA-MB-231 closely map the new claudin-low molecular subtype [6], and clearly these are significantly different in molecular and phenotypic behavior, with MDA-MB-468 being highly proliferative and prognostically highly compromised relative to MDA-MB-231, so it matters gravely which cancer cell line is chosen, and it will also matter as to outcome obtained from any given preclinical study trying to determine the efficacy and responsivity of a particular therapeutic agent against one versus the other cell line, yet basic scientists often slur these together as "triple-negative" cell lines.
Furthermore, MDA-MB-231 cells are characterized more critically by claudin-3 and claudinin-4 downregulation, by low expression of the Ki-67 proliferation marker, enrichment for markers associated with EMT, and, importantly, the expression of features associated with mammary cancer stem cells (CSCs) like the CD44+CD24-/low phenotype. But these features are not shared with MDA-MB-468 [9.10] so we would expect that MDA-MB-468 would be differentially responsive to MEK protein kinase inhibitors among other molecular pathway targeting agents, but not so for MDA-MD-231. What a difference a cell line makes! So we must always make explicit recognition of the fact that MDA-MB-468 is a basal BC cell line versus MDA-MB-231 which is now known to be a claudin-low, not basal, cell line.
THE SECOND GENERATION: THE ERA OF TNBC SUBTYPING
But the third issue is the most critical: we are now in the second generation of TNBC molecular architecture, where the triple negative breast cancer (TNBC) subclass/subgroup is itself decomposed into six distinct subtypes [7,8]:
- two basal-like subtypes, BL1 and BL2, involving cell cycle and DNA damage response genes;
- two mesenchymal subtypes, M and MSL, driven by genes involved in cell differentiation and growth factor pathways;
- an immunomodulatory (IM) type driven by immune system genes, plus
- a luminal subgroup subtype, LAR (luminal androgen receptor ), driven by signaling of the male sex hormone androgen receptor (AR)
CLINICAL IMPLICATIONS OF THE NEW TNBC SUBTYPING MOLECULAR ARCHITECTURE
So the lesson to learn is that preclinical and clinical studies need to become aware of these subgroups. For example, the M and MSL subtypes respond to Src inhibition using dasatinib (Sprycel), in contrast to the BL1 and BL2 subtypes which are not similarly responsive, but rather exhibit some responsivity to the platinum cisplatin. In contrast, the LAR TNBC subtype is responsive to the AR (androgen receptor) antagonist bicalutamide (Casodex) which is showing significant clinical promise outside of metastatic prostate cancer, for AR-positive breast cancer.
But there is another even more critical lesson: the objective response rate (ORR), particularly pCR (pathological complete response) can be vastly different between TNBC subtypes. This was demonstrated in a recent retrospective analysis [11] where it where it was found that although the overall pCR response from neoadjuvant chemotherapy was 28% in a TNBC population, the actual subtype-specific responses differed significantly: thus, pCR was 0% for patients with the BL2 subtype, and just 10% for those with LAR tumors and 23% for MSL subtypes, but in stark contrast the BL1 subtype achieved the highest pCR rate at an exceptional 52%. In addition, a patient's TNBC subtype was demonstrated to be an independent predictor of pCR status under likelihood ratio test.
Thus, we now are beginning to see true clinical relevance emerge from the TNBC molecular subtyping architecture, of both prognostic and therapy-response predictive value, and several other validating clinical studies are currently in press.
HOW TO SUBTYPE TNBC USING THE TNBCtype TOOL
As I deal extensively with advanced disease TNBC patients, I use the TNBCtype subtyping tool - when of course gene expression profiles are available - to capture and map to the true reality of the human molecular level for TNBC and basal subtypes and their subgroups. This freely accessible TNBCtype tool is a rare public service from the Vanderbilt University team that ushered in the TNBC Subtyping Molecular era I briefly described above, and what it provides is a determination TNBC molecular subtype from gene expression profile input, entered as a genome-wide gene expression matrix in the form of a .csv (derivable from Excel and other Office programs) file on the user-friendly web interface TNBCtype website at:
Comprehensive instructions for how to input data into the TNBCtype tool is available, and any residual questions are kindly answered by Stephen Chen (email him at: steven.chen@vanderbilt.edu). Before using the tool, I would strongly advise reading Stephen's paper [8] on TNBCtype, as well as Brian Lehmann's paper on TNBC molecular subtyping [7].
Truly, we've come a long way from the relatively naive early pre-molecular immunohistochemical (IHC) receptor-based classification of TNBC, through the first generation of breast cancer molecular subclassing courtesy of the genius of Charles Perou and Therese Sørlie Stanford University team, and finally through the innovate, ground-breaking TNBC molecular subtyping architecture brought to us by the forward-thinking Vanderbilt University team of Brain Lehmann and Stephen Chen. So in any research project exploring and comparing the luminal (A and B) breast cancer subclasses with TNBC cell lines must be aware and take into account these new and critical facts of TNBC molecular architectures, down to the deep subtyping level.
REFERENCES
1. Perou CM, Sorlie T, Eisen MB, van de Rijn M, Jeffrey SS, et al. (2000) Molecular portraits of human breast tumours. Nature 406: 747–752. doi: 10.1038/35021093.
2. Sorlie T, Perou CM, Tibshirani R, Aas T, Geisler S, et al. (2001) Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications. Proc Natl Acad Sci U S A 98: 10869–10874.
3. Sorlie T, Tibshirani R, Parker J, Hastie T, Marron JS, et al. (2003) Repeated observation of breast tumor subtypes in independent gene expression data sets. Proc Natl Acad Sci U S A 100: 8418–8423.
4. Prat A, Perou CM. Deconstructing the molecular portraits of breast cancer. Mol Oncol 2011; 5(1):5-23.
5. Hennessy, B.T. et al. Characterization of a naturally occurring breast cancer subset enriched in epithelial-to-mesenchymal transition and stem cell characteristics. 2009, Cancer Res., 69, 4116.
6. Prat A, Parker J, Karginova O, Fan C, Livasy C, Herschkowitz JI, He X, Perou CM: Phenotypic and molecular characterization of the claudin-low intrinsic subtype of breast cancer. Breast Cancer Res 2010, 12:R68.
7. Lehmann BD, Bauer JA, Chen X, et al. Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. J Clin Invest 2011 Jul 1; 121(7):2750-67.
8. Chen X, Li J, Gray WH, et al. TNBCtype: A Subtyping Tool for Triple-Negative Breast Cancer. Cancer Inform 2012; 11:147-56.
9. Sheridan C, Kishimoto H, Fuchs RK, et al. CD44+/CD24- breast cancer cells exhibit enhanced invasive properties: an early step necessary for metastasis. Breast Cancer Res 2006; 8(5):R59.
10. Jaggupilli A, Elkord E. Significance of CD44 and CD24 as cancer stem cell markers: an enduring ambiguity. Clin Dev Immunol 2012; 2012:708036.
11. Masuda H, Baggerly KA, Wang Y, et al. Differential response to neoadjuvant chemotherapy among seven triple-negative breast cancer molecular subtypes. Clin Cancer Res 2013; 19(19): 5533–5540.
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Which is the best antiedemigen drug?
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How long ago was the surgery done?is there redness?
I prefer disperzyme in my practice
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The introduction of SLNB has reduced the incidence of lymphedema in patients with node negative axillae but in patients with locally advanced breast cancer patients, ALND is still the standard of care. ARM has shown potential to identify the arm lymph nodes and lymphatics but is it really feasible in patients with LABC?
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Yes
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There are five main methods in breast volume measurement. Although there is no standard method for breast volumetry, volumetry with Grossman-Roudner Disk seems to have some advantages like easiness, simplicity, comfort for the patient and cost.
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Dear Fernandes,
Your method of choosing appropriate prosthesis is a well known and the best one defined by Hidalgo etal,and Tegtmeier.However, breast volume measurement may be useful in following conditions:
a-to define excess or deficient volumes and the degree of asymmetry
b-choosing and planning the most suitable surgical method for the patient,
c-in the evaluation of cosmetic outcome,
d-countless of other benefits in the diagnosis and treatment of breast diseases..
kind regards.RKayar
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Pathological complete response is a very important marker after chemotherapy. I want to understand what is the meaning of it.
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Hamed:
This is an excellent question, still fraught with confusion, controversy and lack of consensus, so I will try below to clarify the issues involved and suggest
DEFINING pCR (PATHOLOGICAL COMPLETE RESPONSE)
TROUBLE IN PARADISE: NO CONSENSUS
The core of any definition of pCR is achieving no residual histological evidence of tumor after chemotherapy at the time of surgery (i.e. a pathological complete response (pCR)). But, past this, as noted by FDA experts Tatiana Prowell and Patricia Cortazar of the FDA's Breast Oncology Group [1], the definition of pCR itself has no universal consensus: it may be construed as:
(1) absence of invasive cancer in the breast only;
OR
(2) absence of invasive cancer in the breast AND axillary lymph nodes;
OR
(3) absence of invasive AND in situ cancer in the breast only;
OR
(4) absence of invasive AND in situ cancer in the breast AND axillary lymph nodes
showing that some investigators evaluate pCR based on the state of the primary lesion alone, whereas others evaluate it based on the states of both the primary lesion and axillary lymph nodes, and investigators are also split has to whether in situ disease (DCIS) is allowed or not.
Furthermore, there is no standard method for grading pathological response of breast tumors to neoadjuvant chemotherapy and a number of different classification systems have been proposed [2,3,4,5,6,7]. Most, but not all, of these grading schemes have included both no residual disease of any sort and residual ductal carcinoma in situ (DCIS) without invasive disease in the definition of pCR, that is, they allowed for residual DCIS as long as there was otherwise no residual histological evidence of tumor.
WHAT A DIFFERENCE A DEFINITION MAKES
A clear demonstration that differences in definition can matter as to what the computed response rates are is given by Frederique Penault-Llorca and colleagues in France [8] who conducted a review of neoadjuvant therapy for 710 breast cancer patients in order to assess the residual disease in breast and nodes according to either the pTNM system of Chevallier [2] as opposed to that of the Sataloff classification [3]. What they found was that the pCR rate is 14.3% according to the pTNM system but almost double that (25.8%) when computed under the Sataloff classification. Why, we ask? This is entirely due to the different definitions of pCR being used: under the pTNM system, pCR is defined as the “disappearance of all invasive tumor” but under the Sataloff classification the definition of pCR is far more relaxed and permissive, being “total therapeutic effect or minimal residual disease (scattered cells accounting for less than 5% of the tumor surface)”.
THE DILEMMA SOLVED
The Royal Marsden team's retrospective analysis of a prospectively maintained database found no difference in disease-free survival (DFS) and overall survival (OS) between patients with residual DCIS and those with no invasive or in situ disease following neoadjuvant chemotherapy for breast cancer [9]. This settles the question as to whether the definition of pCR needs to explicitly include the absence of in situ cancer, and the answer is that it does not, as this does not give rise to any clinically relevant impact on either DFS or OS outcomes. This leaves the definition as "absence of invasive cancer in the breast" (regardless of the presence or absence of any in situ disease), and this brings it essentially in agreement with the NSABP (National Surgical Adjuvant Breast and Bowel Project) definition in their NSABP B 18 trial [4] which allows specimens with intraductal (that is, in situ) residual tumor cells. That leaves, to my mind, only the M.D. Anderson (MDA) Cancer Center trial’s pCR criteria [10] as requiring not only complete response of the primary lesion but also the disappearance of axillary lymph node metastasis, and it strikes me that this is a more radical and not widely adopted criteria (remember: axillary lymph node disease often requires radiotherapy, above and beyond, chemotherapy, to be regressed, so this goes beyond the customary definition of pCR as the consequence of chemotherapy). In addition, if we use the reasonable criteria of:
(1) the most accurate prognosis,
(2) a sufficient number of patients and
(3) thorough follow-up;
then only the NSABP B18 trial pCR definition ("absence of invasive cancer in the breast" (regardless of the presence or absence of any in situ disease)) meets these conditions, but there can still be some divergence in definition here so an interim suggestion is that every study explicitly and clearly provide their definition of pCR so we know what criteria are being used.
WHAT IS STILL NEEDED
However, in conclusion, although the NSABP definition of pCR seems the most compelling, nonetheless there still remains a vital need to adopt a singular cohesive authoritative definition to avoid cross-trial lack of translatability, and that it seems to me requires the authority of an organization like ASCO in conjunction with comparable European, Japanese, and other national, regional and international guideline organizations to finally promulgate a consensus statement to be used across all clinical trials.
REFERENCES
1. Prowell T, Cortazar P. Pathologic Complete Response in Neoadjuvant Treatment of High-Risk Early-Stage Breast Cancer: Use of an Endpoint to Support Accelerated Approval. Office of Hematology Oncology Products Breast Oncology Group. FDA Webinar. June 28, 2012. At: http://www.fda.gov/downloads/Drugs/UCM310088.pdf.
2. Chevallier B, Roche H, Olivier JP, Chollet P, Hurteloup P (1993) Inflammatory breast cancer. Pilot study of intensive chemotherapy (FEC-HD) results in a high histologic response rate. Am J Clin Oncol 16: 223–228.
3. Sataloff DM, Mason BA, Prestipino AJ, Seinige UL, Leiber CP, Baloch Z (1995) Pathologic response to induction chemotherapy in locally advanced carcinoma of the breast: a determinant of outcome. Am J Coll Surg 180: 297–306.
4. Fisher B, Brown A, Mamounas E, Wieand S, Robidoux A, Margolese RG, Cruz AB, Fisher ER, Wickerham DL, Wolmark N, DeCillis A, Hoehn JL, Lees AW, Dimitrov NV (1997) Effect of preoperative chemotherapy on local-regional disease in women with operable breast cancer: findings from the National Surgical Adjuvant Breast and Bowel Project B-18. J Clin Oncol 15: 2483–2493.
5. Honkoop AH, van Diest PJ, de Jong JS, Linn SC, Giaccone G, Hoekman K, Wagstaff J, Pinedo HM (1998) Prognostic role of clinical, pathological and biological characteristics in patients with locally advanced breast cancer. Br J Cancer 77: 621–626,
6. Kuerer HM, Newman LA, Buzdar AU, Dhingra K, Hunt KK, Buchholz TA, Binkley SM, Strom EA, Ames FC, Ross MI, Feig BW, McNeese MD, Hortobagyi GN, Singletary SE (1998) Pathologic tumour response in the breast following neoadjuvant chemotherapy predicts axillary lymph node status. Cancer J Sci Am 4: 230–236.
7. Ogston KN, Miller ID, Payne S, Hutcheon AW, Sarkar TK, Smith I, Schofield A, Heys SD (2003) A new histological grading system to assess response of breast cancers to primary chemotherapy: prognostic significance and survival. Breast 12: 320–327.
8. Penault-Llorca F, Abrial C, Raoelfils I, et al. Comparison of the prognostic significance of Chevallier and Sataloff’s pathologic classifications after neoadjuvant chemotherapy of operable breast cancer. Hum Pathol. 2008;39(8):1221-1228.
9. Jones RL, Lakhani SR, Ring AE, Ashley S, Walsh G, Smith IE. Pathological complete response and residual DCIS following neoadjuvant chemotherapy for breast carcinoma. Br J Cancer 2006 Feb 13; 94(3):358-62.
10. Green MC, Buzdar AU, Smith T et al (2005) Weekly paclitaxel improves pathologic complete remission in operable breast cancer when compared with paclitaxel once every 3 weeks. J Clin Oncol 23:5983–5992.
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Does anybody have any experience with training for adolescents after surgery for pectus excavatum?
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Dear Nelson, I am sorry but I have to disagree with you as far as funnel chest correction is concerned. Unfortunately, conservative treatment (orthoses, exercises, respiratory gymnastics, etc.) may only contribute to improving the general status but not the local deformity. Usually, the pars anterior of diaphragma is too short as a congenital anomaly at birth and this is a sort of rigid rein that pulls the sternum inwards. Especially, in the prepubertal phase of growth the deformity gets deeper and deeper. There are different grades of pectus excavatum. Of course the light forms should not be treated surgically because they represent just a cosmetic defect. Unfortunately, there are severe grades and forms which restrict the respiratory function, displace the heart and cause severe functional problems (i.e. Marfan syndrome). These cases are indicated for surgical correction. The results are good, although sometimes serious complications happen. We use for many years the classic Ravitch procedure in combination with transverse plates to keep the correction untill the healing of the sternum occurs (usually 1 year after the operation). After that we remove the plates.
  • asked a question related to Breast Surgery
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Do we need to clear the tissue between the two veins and the incidence of lymphedema in these cases?
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Actually, a duplicated axillary vein is a more common occurrence practically than theoretically. There is no literature to suggest the guideline for extent of axillary dissection in such cases. Nor is there any data on incidence of lymphedema. But I reviewed the anatomical basis of a duplicated axillary vein and that gave me some clue as to the extent of axillary dissection which i now follow in my clinical practice. Axillary vein normally is formed as a result of the union of the basilic vein and the vennae commitantes of the brachial artery. In a duplicated state, the vennae commitantes fuse to form the antero-inferior axillary vein and the basilic continues as the postero-superior axillary vein.Nodes along the basilic vein are known to drain lymph solely from the upper limb outer half and hence do not contribute to lymphatic clearance for the breast. it thus stands to reason that the anteroinferior axillary vein should be treated as the main axillary vein in the duplicated state and the tissue in between left alone. Its an excellent question and any further comments would be welcome
  • asked a question related to Breast Surgery
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I like to know about the statistical figures and the sites of recurrence/secondary cancer development after surgical removal of tumor in breast. How its managed if this occurs?
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There was a study published in the BMJ this year (Jeevan et al I think) looking at recurrence rates following surgery. They quoted a 30% recurrence rate following WLE...
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I am going to assess the patients discomfort while performing ROLL and compare it to wire guided localisation.
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Dear Mercieca,
you can compare following items in your study:
a-The duration of procedures(under local and/or general anesthesia and total time)
b-patient opinion about them:(painstaking,bothering,unacceptable,acceptable,quite acceptable....e.g)
c-Physician's(user's) opinion about easiness of procedures(difficult,moderate and easy)
d-the cost of procedures..
These factors may give better understanding about the discomfort of each modality...
kind regards
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I'm reading on the medical reviews for TNBC and I'm a little bit confused with these terms.
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Given that there have been no international consensus standards for the definition of survival end points used in clinical trials and supporting literature, Adam Olszewski is to be much thanked for citing, above, the STEEP system, a major step in the right direction, although not on its own enough, and not (yet) adopted by ASCO, NCI or other authorities, and, regrettably, rather inconsistently used - when used at all - in the oncology literature.
In the adjuvant setting the ‘STEEP’ system as introduced by Cliff Hudis at Memorial Sloan-Kettering and colleagues [1] - must reading for any serious researcher - defines the events contributing to survival endpoints, but note that this is solely for the adjuvant setting - that is the reason in fact that no definition is given for progression-free survival (PFS) and other non-adjuvant endpoints. A joint working group of members from both BIG (the Breast International Group) and NABCG (the North American Breast Cancer Group) is currently undertaking a similar but more expansive effort that includes advanced/metastatic setting endpoints and collaborative initiatives (which I am myself involved in) are addressing the issue aggressively at this time [2], for reasons I will make clear below.
Some Survival Endpoint Definitions
But first the definitions. Distilling these proposals (STEEP and BIG/NABCG [private communication]), I present the following proposed working definitions of survival endpoints, relativized for the sake of this discussion to the breast cancer context (to generalize the definition just substitute "disease" for "breast cancer"):
Recurrence-free survival (RFS) includes (1) any recurrence (local or regional [including invasive ipsilateral tumor and invasive locoregional tumor], or distant) and (2) death due to any cause (both BC and non-BC causes of death). Note that under STEEP DFS (disease-free survival) is interchangeable with recurrence-free survival.
Relapse–free survival is defined as any disease recurrence (local, regional, or distant), but death is censored (not included). So recurrence-free survival includes all-cause death which relapse free-survival does not, as seen in the formal definition of relapse-free survival used in the landmark TNBC studies such as Rebecca Dent's: "the time of diagnosis to development of first evidence of clinical or radiographic metastatic disease" [3], among others.
Progression-free survival (PFS) is defined as the time elapsed between treatment initiation and (1) metastatic tumor progression - but note NOT local or regional progression - or (2) death from any cause, with censoring of patients who are lost to follow-up (see [4], and numerous others to same effect). With PFS therefore we are concerned only with distant, not locoregional, disease progression, and with death from any cause (like RFS (recurrence-free survival)).
Finally, time to progression (TTP) differs from PFS solely in that the event of interest is only disease progression, so it does not include death from non-BC causes.
The Problem: Lack of Consensus
However, be aware that even years after the STEEP proposal, there is still wide inconsistency across the literature in the use of these definitions. So for example, 13 of 16 studies recently reviewed [5] counted death as an event in treating TTP, making TTP indistinguishable from PFS, leading the reviewers to conclude that "The lack of uniformity regarding the definition of end points may lead to miscommunication and to confusion when results of different trials are compared, and uniform adoption of the definitions seems therefore in order".
Similarly, in a systematic review [6] of 125 articles that included primary analyses of RCT with survival end points, it was found that clear definitions of the survival end point used were not provided in almost half (48%) of these papers, and 68% reported insufficient information of the survival analysis altogether. And another review [7] demonstrated that whether contralateral breast cancer or non-disease (non-BC) related death was included or excluded in the relevant endpoint definitions significantly affected the estimated outcome probability, making a clinically relevant difference in the conclusions derivable from major trial such as the ATAC Trial (comparing tamoxifen with anastrozole).
Another Plea for Survival Endpoint Standards
This is clearly a wholly unacceptable situation in a medical science that pretends to methodological rigor research integrity, and it is long overdue that standards authorities, as I and others have been calling for years, finally issue comprehensive guidelines for the consistent use of survival endpoints, and that journals aid this initiative in demanding clear and standard definitions for any and all survival endpoints and analyses used in any study submitted for publication.
References
1. Hudis CA, Barlow WE, Costantino JP, et al. Proposal for standardized definitions for efficacy end points in adjuvant breast cancer trials: the STEEP system. J Clin Oncol 2007;25(15):2127-2132.
2. Bartsch R, Dubsky PC, Loibl S, Steger G. Opinions on the ASCO 2011 Annual Meeting. Breast Care (Basel) 2011; 6(4):315-319.
3. Dent R, Trudeau M, Pritchard KI, et al. Triple-negative breast cancer: clinical features and patterns of recurrence. Clin Cancer Res 2007 Aug 1; 13(15 Pt 1):4429-34.
4. Green S, Benedetti J, Crowley J. Clinical Trials in Oncology. London: Chapman & Hall; 1997. p. 40.
5. Saad ED, Katz A. Progression-free survival and time to progression as primary end points in advanced breast cancer: often used, sometimes loosely defined. Ann Oncol 2009; 20(3):460-4.
6. Mathoulin-Pelissier S, Gourgou-Bourgade S, Bonnetain F, Kramar A. Survival end point reporting in randomized cancer clinical trials: a review of major journals. J Clin Oncol 2008 Aug 1; 26(22):3721-6.
7. Nout RA, Fiets WE, Struikmans H, Rosendaal FR, Putter H, Nortier JW. The in- or exclusion of non-breast cancer related death and contralateral breast cancer significantly affects estimated outcome probability in early breast cancer. Breast Cancer Res Treat 2008; 109(3):567-72.
Constantine Kaniklidis
Director of Medical Research,
No Surrender Breast Cancer Foundation (NSBCF)
European Association for Cancer Research (EACR)